Download Feline leukaemia virus: a review

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

African trypanosomiasis wikipedia , lookup

Leptospirosis wikipedia , lookup

Influenza A virus wikipedia , lookup

2015–16 Zika virus epidemic wikipedia , lookup

Eradication of infectious diseases wikipedia , lookup

HIV wikipedia , lookup

Norovirus wikipedia , lookup

Human cytomegalovirus wikipedia , lookup

Hepatitis C wikipedia , lookup

Chickenpox wikipedia , lookup

Orthohantavirus wikipedia , lookup

Ebola virus disease wikipedia , lookup

Middle East respiratory syndrome wikipedia , lookup

Dirofilaria immitis wikipedia , lookup

Antiviral drug wikipedia , lookup

Herpes simplex virus wikipedia , lookup

Marburg virus disease wikipedia , lookup

Pandemic wikipedia , lookup

West Nile fever wikipedia , lookup

Hepatitis B wikipedia , lookup

Henipavirus wikipedia , lookup

Lymphocytic choriomeningitis wikipedia , lookup

Transcript
Surveillance Vol.14 No.2 1987
Feline leukaemia virus: a review
Feline leukaemia virus ( F e L v is a
contagious viral disease of cats which
can affect the large cats as well as Felis
domestica. It can cause severe illness
and death in the domestic cat, but is
only infrequently associated with disease in exotic feline species.'
The disease agent belongs to the
large family of retroviruses which
includes, among other, the viruses
causing bovine leucosis, avian
leucosis, and AIDS (acquired immunodeficiency syndrome of man).
Synonyms for FeLV are C-type
virus, oncornavirus.
Symptoms
FeLV causes a wide spectrum of diseases, including proliferative diseases
such
as
leukaemia
and
lymphosarcoma and degenerative syndromes such as anaemia and immunosuppression. It is thus referred to as
the feline leukaemia complex.
The clinical signs are jaundice,
depression, appetite loss, weight loss,
diarrhoea or constipation, enlarged
lymph nodes, respiratory distress, the
fading kitten syndrome, polydipsia,
abortion, and infertility.
Half the diagnosed cases of feline
infectious peritonitis have been found
to have FeLV antibodies.',2 This
results from the immunosuppression
caused by FeLV, which lessens the
resistance of the host to other viruses.
There are three possible outcomes
of FeLV infection:
1 In the majority of cases, there is the
development
of
neutralising
antibodies, resulting in rapid elimination of the virus and complete
recovery.
2 Some cats develop a persistent
viraemia which may become established in the absence of a detectable
neutralising antibody response, and
which is related to a high possibility of future occurrence of an
FeLV-related disease.
3 The infection may remain latent.
In such instances there is no virus
in the blood, but the virus is present in the bone marrow cells.
Antibody titres are similar to those
of animals which have completely
eliminated the virus. Large doses of
corticosteroids may reactivate the
virus and result in ~ i r a e m i a . ~
Transmission
Retroviruses are transmitted both
vertically and horizontally.
Early studies into FeLV suggested
that is was mainly transmitted vertically. Recent research shows that horizontal transmission is most important
in FeLV infections, as not all infected
queens transmit virus to their kittens
in utero. The virus is found especially
in saliva and urine from virally
infected cats.3 Viraemic clinically
healthy cats can provide a constant
source of infection over many years.
Kittens may be infected via the
queen's milk. They seem to have passive protection for the first few weeks
of life but become viraemic after
about 45 days.4
Virus transmission occurs almost
exclusively by direct contact. The
virus enters the nasal or oral cavities.
It replicates in the local lymph nodes
and can be briefly detected in the
bloodstream in mononuclear cells.
The infection then spreads to other
lymphoid organs such as the spleen
and lymph nodes, and to the intenstine and bladder mucosa.
In many cats the virus infects the
bone marrow, where it grows in the
stem cells of the platelets, leukocytes,
and erythrocytes. This occurs several
weeks after infection, and at the same
time viral antigens appear in the
mature blood cells. Cats at this stage
Table 1: Prevdence of FeLV in New Zealand
Laboratory
It
Christchurch . .
..
..
R u h
..
..
Palmemton N&
.
..
Palmemton North Lab survey.
..
Whangarei ..
..
..
TOTAL
..
..
..
Minus survey*
..
..
* Survey carried out by the lab was biased.
.
..
..
..
..
..
..
..
..
..
..
..
..
..
..
No. of
cats tested
156
79
149
104
463
95 1
847
No. identified
as positive
AI
13 (8.7%)
21 (20.2%j
28 16.0%)
73 (7.7%)
52 (6.1%)
are usually positive to the indirect fluorescent antibody test (IFAl From the
bone marrow, virus enters the bloodstream, causing viraemia, and virus
excretion f01lows.~
Prevalence
The prevalence varies throughout
the world, but tends to be higher in
multi-cat colonies, for obvious reasons. While the number of animals
affected with FeLV is probably less
than 3% in most healthy cat populations, the numbers which have been
exposed to challenge from the virus
may be up to 40%3 and may reach
100%.
There is a higher prevalence in kittens because of the close contact and
the risk of vertical transmission, and
in older cats which may have a compromised immune system.
Frequent contact with healthy cats
shedding virus puts animals at risk,
even those from single-cat households.
Those singletons most at risk are cats
which have free access outdoors.
Some investigations show increased
prevalence during warmer weather,
but this may be due not only to survival of the virus, but to cats' habits.
Other studies suggest more cats are
affected during cold weather and associate this with stress.6
Results from testing at MAF
Animal Health Laboratories are
shown in table 1.
Separate surveys camed out by
Massey University showed prevalence
of 4.4%-6.45%,' which is similar to
that shown in table 1.
These figures cannot be quoted as
representative of the cat population in
New Zealand because the samples are
biased. In most cases tests are performed on those animals suspected of
the diseases and in routine testing of
breeding catteries.
Assessing the importance of FeLV
in New Zealand is difficult because of
the lack of data. There is no record of
the number of cats, and studies of the
Surveillance 14 (2) 9
Surveillance Vol.14 No.2 1987
disease have been in isolated pockets.
If we accept a rule of thumb based on
urban surveys camed out by the
SPCA, there are between 2.1 and 2.8
cats per household, and from that a
conservative estimate is that there are
over two million cats in New Zealand.
Assuming the MAF Animal Health
Laboratories service 25% of these, it
would appear that the prevalence of
FeLV here is low.
So far there is no evidence in New
Zealand of seasonal effects, or the
association of breed, colour, or sex.
Diagnosis
There are three methods of testing
for FeLV. The IFA, the enzyme-linked
immunosorbent assay (ELISA), and
virus isolation. Overall the ELISA
shows a higher proportion of positives
than the IFA. All three tests have good
agreement on negative animals.
MAFQual Animal Health Laboratories offer an ELISA test for FeLV. All
laboratories provide the service,
although not all perform the test themselves. The ELISA appears to be more
sensitive than the IFA and to provide
a means of identifying animals earlier
in the course of infection.
Some ELISA-positive animals may
belong to the first group mentioned
above, which successfully eliminate
the virus. So cats which are ELISA
positive should not be immediately
destroyed but should be isolated from
negative animals and retested 12
weeks later.
Testing with IFA does not add more
information on the cat’s disease status
than repeat ELISA t e ~ t i n g . ~
Control and vaccination
Control of FeLV relies on identifying camer or infected animals and
preventing infected cats from
mingling with non-infected ones.
FeLV has been difficult to manage
clinically. The first vaccines that were
trialed were inactivated/killed types
and some resulted in vaccinated animals being more susceptible to disease
than controls. This was thought to be
related to an immunosuppressiveprotein in FeLV which interfered with the
feline immune systern.l0 The vaccines
contained killed FeLV, but a toxic
peptide remained, and even in small
quantities it cancelled lymphocytic
function.
Recently a vaccine has been made
from soluble tumour proteins which
do not contain the toxic factor. This
vaccine has proved efficacious. Known
as STAV (soluble tumour antigen vaccine), the vaccine does not interfere
with currently available laboratory
tests and has not proved to have side
effects. It may be used prophylactically in eradicting disease from breeding establishments, though it has not
been shown to reverse the disease in
infected cats. Test information is useful though not a prerequisite for
vaccination.
10 Surveillance 14 (2)
Vaccination will probably become
one of the routine feline vaccinations
for breeding colonies and for certain
multi-cat establishments in areas
where FeLV is known to occur and
where new animals are frequently
introduced.
Difficult parameters
The situation is less clear for singlecat households. It will depend on the
access the cat has to the outdoors, the
proximity of other cats, and the percentage of infected cats in the population. These are difficult parameters to
measure.
The vaccine available in New Zealand is a killed vaccine. The question
of whether to test animals prior to
vaccination remains. The vaccine has
no side effects, so vaccination will do
no harm to infected animals but is
unlikely to benefit them either. It
remains to the discretion of the individual veterinary surgeon, taking into
account the:
0 cat’s value to its owners;
0 cost of the vaccine;
0 likelihood of the cat’s already being
affected;
0 likely exposure of the cat to
infected animals;
serious nature of the disease in clinically affected animals.
References
Briggs, M B, Ott, R L, 1986: “Feline leukaemia virus infection in a captive cheetah and
the clinical and antibody response of six cap
tive cheetahs to vaccination with a subunit
feline leukaemia virus vaccine.” JA VMA,
Vol. 189, No. 9.
Jubb, Jennifer Causey, 1982: “Feline infectious peritonitis: a review” Veterinary
Medicine/SmaN Animal Clinician, November, pp 1631-1634.
Jarrett, W T H, et al. 1973: “Horizontal
transmission of leukaemia virus and leukaemia in the cat” J. National Cancer Institute,
51:833 (referred to by Olsen, Richard G ,
1985: “An innovative technique produces a
feline leukaemia virus vaccine.” Veterinary
Medicine, January.)
Pacitti, A M, Jarrett, 0, Hay, D ,1986:
“Transmission of feline leukaemia wrus in
the milk-of a non-virakic cat” Veterinary
Record, 5 April, p 38 1.
Moennig, Voker, 1986: “Feline leukaemia
prohpylaxis.” Felinfo 2, J. Small Anim. Pract:
345-352.
McMichael, J C, Stiers, S, Cofin, S, 1986
“Prevalence of feline leukaemia virus infection among adult cats at an animal control
centre: association of viraemia with phenotype and season.”Am. J. Res, Vol. 47, No. 4,
April.
Jones, B R, Lee, E A and Pauli, J V, 1982:
“Feline leukaema wrus testing.” NZ Vet. J.,
30: 161.
Gary Homer, Ruakura Animal Health Laboratory, 1987: personal communication.
Jones, B R, Lee, E A, 1981: “Feline leukaemia virus testing.” NZ Vet, J.. 29: 188-1 89.
10 Mathes, L E, ethl. 1978 “Abrogation of the
lymphocyte blastogenesis by a feline leukaemia virus protein.” Nature, .274:687.
Gabnelle George, Veterinary Staff Officer
MAFOual. Head Office